Dual antiplatelet therapy (DAPT) with aspirin and a P2Y inhibitor is a mainstay of the prevention of stent thrombosis following percutaneous coronary intervention (PCI). In the 2015 European guidelines for the management of acute coronary syndrome (ACS), prasugrel (PRA) and ticagrelor (TICA) combined with aspirin are recommended as first-line therapy. Clopidogrel (CLO) is recommended as an alternative medication for patients with contradictions to these new drugs. This single-center study analyzed the platelet function of 809 ACS patients undergoing PCI and treatment with DAPT. The platelet response to ADP was determined using Multiplate® analyzer at a median of 3 days after PCI in 254 patients treated with PRA (loading dose [LD] 60 mg, 10 mg qd), 162 patients receiving TICA (LD 180 mg, D 90 mg bid), and 393 CLO-treated patients (LD 600 mg, 75 mg qd). An aggregation >468 arbitrary units (AU)*min was defined as "high on-treatment platelet reactivity" (HPR), <188 AU*min as "low on-treatment platelet reactivity" (LPR). Platelet response in PRA-treated patients was lower compared to CLO or TICA (median; interquartile range: PRA 220 [163-275] AU*min vs. CLO 268 [186-387] AU*min, p < 0.001 vs. TICA 245 [190-320] AU*min, p = 0.001). Only 1.6% of PRA patients were stratified as HPR and 34.6% as LPR, while in the TICA group 1.9% fulfilled the criteria of HPR and 24.1% criteria of LPR. Sixteen percent of CLO patients were stratified as HPR and 26.2% as LPR. In a real-world cohort of ACS patients following PCI, PRA results in more potent inhibition of platelet function compared to CLO and TICA. TICA achieves a consistent antiplatelet effect with reduced rates of HPR and LPR in relation to CLO.

Dear Sirs, Oxidised low-density lipoprotein (oxLDL) is crucially involved in thrombotic disease and progression of atherosclerotic plaques by activating inflammatory cells such as platelets (1, 2) and by transforming monocytes and macrophages into proatherogenic foam cells (3, 4). Currently there have been described four major scavenger receptors on platelets: SR-A, CD36, Lox-1 and SR-BI (2, 5-7). To the best of our knowledge, the scavenger receptor for phosphatidylserine and oxidised lipoprotein SR-PSOX/CXCL16 (henceforth referred to as CXCL16) has not been described on platelets so far. CXCL16 is a unique protein that functions as an endocytotic receptor or adhesion receptor when it is expressed on cell membranes of dendritic cells or macrophages or as a chemokine when it is released into the extracellular space (8-11). CXCL16 could act as an attractant and adhesion molecule for CXCR6-expressing T-cells which could contribute to disease development of atherosclerosis (12). Recently it has been reported that soluble CXCL16 in patient plasma can serve as a biomarker for acute coronary syndromes (13). Based on the fact that platelets are essentially involved in acute coronary syndrome (ACS), we investigated the expression of CXCL16 on platelets and its expression in patients with coronary artery disease (CAD). First we analysed the mRNA expression and surface expression of CXCL16 in / on platelets. In fact, platelets express CXCL16 at mRNA (ǠFig.

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